VSTM1-v2 does not drive human Th17 cell differentiation: A replication study

Signal inhibitory receptor on leukocytes-1 (SIRL-1) is an immune inhibitory receptor expressed on human myeloid cells. We previously showed that dendritic cell (DC)-driven Th17 cell differentiation of human naive CD4(+) T cells requires presence of neutrophils, which is inhibited by SIRL-1 ligation....

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Autores principales: von Richthofen, Helen J., Hafkamp, Florianne M. J., van Haperen, Anouk, de Jong, Esther C., Meyaard, Linde
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2023
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10101491/
https://www.ncbi.nlm.nih.gov/pubmed/37053248
http://dx.doi.org/10.1371/journal.pone.0284404
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author von Richthofen, Helen J.
Hafkamp, Florianne M. J.
van Haperen, Anouk
de Jong, Esther C.
Meyaard, Linde
author_facet von Richthofen, Helen J.
Hafkamp, Florianne M. J.
van Haperen, Anouk
de Jong, Esther C.
Meyaard, Linde
author_sort von Richthofen, Helen J.
collection PubMed
description Signal inhibitory receptor on leukocytes-1 (SIRL-1) is an immune inhibitory receptor expressed on human myeloid cells. We previously showed that dendritic cell (DC)-driven Th17 cell differentiation of human naive CD4(+) T cells requires presence of neutrophils, which is inhibited by SIRL-1 ligation. VSTM1-v2 is a soluble isoform of SIRL-1, which was previously proposed to function as a Th17 polarizing cytokine. Here, we investigated the effect of VSTM1-v2 on DC-driven Th17 cell development. Neutrophils induced DC-driven Th17 cell differentiation, which was not enhanced by VSTM1-v2. Similarly, we found no effect of VSTM1-v2 on cytokine-driven Th17 cell development. Thus, our results do not support a role for VSTM1-v2 in Th17 cell differentiation.
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spelling pubmed-101014912023-04-14 VSTM1-v2 does not drive human Th17 cell differentiation: A replication study von Richthofen, Helen J. Hafkamp, Florianne M. J. van Haperen, Anouk de Jong, Esther C. Meyaard, Linde PLoS One Research Article Signal inhibitory receptor on leukocytes-1 (SIRL-1) is an immune inhibitory receptor expressed on human myeloid cells. We previously showed that dendritic cell (DC)-driven Th17 cell differentiation of human naive CD4(+) T cells requires presence of neutrophils, which is inhibited by SIRL-1 ligation. VSTM1-v2 is a soluble isoform of SIRL-1, which was previously proposed to function as a Th17 polarizing cytokine. Here, we investigated the effect of VSTM1-v2 on DC-driven Th17 cell development. Neutrophils induced DC-driven Th17 cell differentiation, which was not enhanced by VSTM1-v2. Similarly, we found no effect of VSTM1-v2 on cytokine-driven Th17 cell development. Thus, our results do not support a role for VSTM1-v2 in Th17 cell differentiation. Public Library of Science 2023-04-13 /pmc/articles/PMC10101491/ /pubmed/37053248 http://dx.doi.org/10.1371/journal.pone.0284404 Text en © 2023 von Richthofen et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
von Richthofen, Helen J.
Hafkamp, Florianne M. J.
van Haperen, Anouk
de Jong, Esther C.
Meyaard, Linde
VSTM1-v2 does not drive human Th17 cell differentiation: A replication study
title VSTM1-v2 does not drive human Th17 cell differentiation: A replication study
title_full VSTM1-v2 does not drive human Th17 cell differentiation: A replication study
title_fullStr VSTM1-v2 does not drive human Th17 cell differentiation: A replication study
title_full_unstemmed VSTM1-v2 does not drive human Th17 cell differentiation: A replication study
title_short VSTM1-v2 does not drive human Th17 cell differentiation: A replication study
title_sort vstm1-v2 does not drive human th17 cell differentiation: a replication study
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10101491/
https://www.ncbi.nlm.nih.gov/pubmed/37053248
http://dx.doi.org/10.1371/journal.pone.0284404
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